Rodríguez-Rivera Carmen, Pérez-Carrión María Dolores, Olavarría Lucía Casariego, Alguacil Luis F, Mora María José Polanco, González-Martín Carmen
Facultad de Farmacia, Universidad CEU San Pablo, Alcorcón, Madrid, Spain.
Facultad de Medicina, Universidad de Castilla-la Mancha, Albacete, Spain.
Food Nutr Res. 2021 May 4;65. doi: 10.29219/fnr.v65.5709. eCollection 2021.
Food-related disorders are increasingly common in developed societies, and the psychological component of these disorders has been gaining increasing attention. Both overnourishment with high-fat diets and perinatal undernourishment in mice have been linked to a higher motivation toward food, resulting in an alteration in food intake. Clusterin (CLU), a multifaced protein, is overexpressed in the (NAc) of over-fed rats, as well as in those that suffered chronic undernutrition. Moreover, an increase of this protein was observed in the plasma of obese patients with food addiction, suggesting the implication of CLU in this eating disorder. To characterize CLU's cellular mechanisms, experiments of undernutrition were performed using dopaminergic SH-SY5Y cells. To mimic dietary conditions, cells were treated with different fetal bovine serum (FBS) concentrations, resulting in control (C group) diet (10% FBS), undernourishment (U group) diet (0.5% FBS), and undernourishment diet followed by restoration of control diet (UC group) (0.5 + 10% FBS). Undernourishment compromised cell viability and proliferation, and concomitantly increased CLU secretion as well as the cytosolic pool of the protein, while decreasing the mitochondrial level. The restoration of normal conditions tended to recover cell physiology, and the normal levels and distribution of CLU. This research study is a step forward toward the characterization of clusterin as a potential marker for food addiction and nutritional status.
与食物相关的失调在发达社会中越来越普遍,这些失调的心理成分也越来越受到关注。小鼠的高脂肪饮食过度营养和围产期营养不足都与对食物的更高动机有关,导致食物摄入量发生改变。聚集素(CLU)是一种多面蛋白,在过度喂养大鼠的伏隔核(NAc)以及那些遭受慢性营养不足的大鼠中过度表达。此外,在患有食物成瘾的肥胖患者血浆中观察到这种蛋白增加,表明CLU与这种饮食失调有关。为了表征CLU的细胞机制,使用多巴胺能SH-SY5Y细胞进行了营养不足实验。为了模拟饮食条件,用不同浓度的胎牛血清(FBS)处理细胞,产生对照(C组)饮食(10% FBS)、营养不足(U组)饮食(0.5% FBS)以及营养不足饮食后恢复对照饮食(UC组)(0.5 + 10% FBS)。营养不足损害了细胞活力和增殖,并同时增加了CLU分泌以及该蛋白的胞质池,同时降低了线粒体水平。恢复正常条件倾向于恢复细胞生理以及CLU的正常水平和分布。这项研究朝着将聚集素表征为食物成瘾和营养状况的潜在标志物迈出了一步。